9 results on '"Junxia Li"'
Search Results
2. HBV-Associated Postinfectious Acute Glomerulonephritis: A Report of 10 Cases.
- Author
-
Yong Zhang, Junxia Li, Weihua Peng, Guoqing Yu, Liping Wang, Jian Chen, and Feng Zheng
- Subjects
Medicine ,Science - Abstract
Postinfectious acute glomerulonephritis (PIGN) may occur after various bacterial and viral infections. Hepatitis B virus (HBV) infection is a cause of chronic glomerulonephritis. We report here 10 cases (ages 7-20 years-old) of chronic HBV carriers with acute glomerulonephritis, with positive glomerular staining of hepatitis B surface antigen, and detectable presence of HBV DNA in the glomeruli. This form of PIGN, HBV-PIGN, has not been previously identified. To further characterize clinical and pathological features of HBV- PIGN, we selected 10 cases of age-matched non-HBV PIGN for comparison. While both HBV associated PIGN and non-HBV PIGN similarly presented as proteinuria, hematuria, and hypertension, there was a trend of higher acute kidney injury and worsened prognosis in HBV-PIGN. 6 months after the onset, 4 patients with HBV associated PIGN did not show improvement from the disease, whereas all patients with non-HBV PIGN had complete or partial recovery. Pathologically, both HBV associated PIGN and non-HBV PIGN showed typical diffuse glomerular endocapillary proliferation, but HBV associated PIGN differed from classical PIGN with much fewer sub-epithelial glomerular "hump-shape" immune complex depositions. In conclusion, we have identified a novel association of HBV infection with acute glomerulonephritis.
- Published
- 2016
- Full Text
- View/download PDF
3. Intravascular ultrasound observation of the mechanism of no-reflow phenomenon in acute myocardial infarction.
- Author
-
Junxia Li, Longmei Wu, Xinli Tian, Jian Zhang, and Yujie Shi
- Subjects
Medicine ,Science - Abstract
To study the mechanism of the no-reflow phenomenon using coronary angiography (CAG) and intravascular ultrasound (IVUS).A total of 120 patients with acute myocardial infarction (AMI) who successfully underwent indwelling intracoronary stent placement by percutaneous coronary intervention (PCI). All patients underwent pre- and post-PCI CAG and pre-IVUS. No-reflow was defined as post-PCI thrombolysis in myocardial infarction (TIMI) grade 0, 1, or 2 flow in the absence of mechanical obstruction. Normal reflow was defined as TIMI grade 3 flow. The pre-operation reference vascular area, minimal luminal cross-sectional area, plaque cross-sectional area, lesion length, plaque volume and plaque traits were measured by IVUS.The no-reflow group was observed in 14 cases (11.6%) and normal blood-flow group in 106 cases (89.4%) based on CAG results. There was no statistically significant difference in the patients' medical history, reference vascular area (no-flow vs. normal-flow; 15.5 ± 3.2 vs. 16.2 ± 3.3, p > 0.05) and lesion length (21.9 ± 5.1 vs. 19.5 ± 4.8, p > 0.05) between the two groups. No-reflow patients had a longer symptom onset to reperfusion time compared to normal blood-flow group [(6.6 ± 3.1) h vs (4.3 ± 2.7) h; p < 0.05] and higher incidence of TIMI flow grade < 3 (71.4% vs 49.0%, p < 0.05). By IVUS examination, the no-reflow group had a significantly increased coronary plaque area and plaque volume compared to normal blood-flow group [(13.7 ± 3.0) mm2 vs (10.2 ± 2.9) mm2; (285.4 ± 99.8) mm3 vs (189.7 ± 86.4) mm3; p < 0.01]. The presence of IVUS-detected soft plaque (57.1% vs. 24.0%, p < 0.01), eccentric plaque (64.2% vs. 33.7%, p < 0.05), plaque rupture (50.0% vs. 21.2%, p < 0.01), and thrombosis (42.8% vs. 15.3%) were significantly more common in no-reflow group.There was no obvious relationship between the coronary risk factors and no-reflow phenomenon. The symptom onset to reperfusion time, TIMI flow grade before stent deployment, plaque area, soft plaques, eccentric plaques, plaque rupture and thrombosis may be risk factors for the no-reflow phenomenon after PCI.
- Published
- 2015
- Full Text
- View/download PDF
4. FSH modulates PKAI and GPR3 activities in mouse oocyte of COC in a gap junctional communication (GJC)-dependent manner to initiate meiotic resumption.
- Author
-
Junxia Li, Guankun Mao, and Guoliang Xia
- Subjects
Medicine ,Science - Abstract
Many studies have shown that cyclic adenosine-5'-monophosphate (cAMP)-dependent protein kinase A (PKA) and G-protein-coupled receptor 3 (GPR3) are crucial for controlling meiotic arrest in oocytes. However, it is unclear how gonadotropins modulate these factors to regulate oocyte maturation, especially by gap junctional communication (GJC). Using an in vitro meiosis-arrested mouse cumulus-oocyte complex (COC) culture model, we showed that there is a close relationship between follicle-stimulating hormone (FSH) and the PKA type I (PKAI) and GPR3. The effect of FSH on oocyte maturation was biphasic, initially inhibitory and then stimulatory. During FSH-induced maturation, rapid cAMP surges were observed in both cumulus cells and oocyte. Most GJC between cumulus cells and oocyte ceased immediately after FSH stimulation and recommenced after the cAMP surge. FSH-induced maturation was blocked by PKAI activator 8-AHA-cAMP. Levels of PKAI regulatory subunits and GPR3 decreased and increased, respectively, after FSH stimulation. In the presence of the GJC inhibitor carbenoxolone (CBX), FSH failed to induce the meiotic resumption and the changes in PKAI, GPR3 and cAMP surge in oocyte were no longer detected. Furthermore, GPR3 was upregulated by high cAMP levels, but not by PKAI activation. When applied after FSH stimulation, the specific phosphodiesterase 3A (PDE3A) inhibitor cilostamide immediately blocked meiotic induction, regardless of when it was administered. PKAI activation inhibited mitogen-activated protein kinase (MAPK) phosphorylation in the oocytes of COCs, which participated in the initiation of FSH-induced meiotic maturation in vitro. Just before FSH-induced meiotic maturation, cAMP, PKAI, and GPR3 returned to basal levels, and PDE3A activity and MAPK phosphorylation increased markedly. These experiments show that FSH induces a transient increase in cAMP levels and regulates GJC to control PKAI and GPR3 activities, thereby creating an inhibitory phase. After PDE3A and MAPK activities increase, meiosis resumes.
- Published
- 2012
- Full Text
- View/download PDF
5. Involvement of an ABI-like protein and a Ca2+-ATPase in drought tolerance as revealed by transcript profiling of a sweetpotato somatic hybrid and its parents Ipomoea batatas (L.) Lam. and I. triloba L
- Author
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Licong Jia, Cancan Zhu, Wang Yannan, Guohong Yang, Shaozhen He, Yang Yufeng, Na Qin, Junxia Li, Dai Xiaodong, Qingchang Liu, Hong Zhai, and Xu Xinzhi
- Subjects
0106 biological sciences ,0301 basic medicine ,Genetic Screens ,Molecular biology ,Cell Membranes ,Gene Identification and Analysis ,lcsh:Medicine ,Gene Expression ,Plant Science ,Biochemistry ,01 natural sciences ,Polyethylene Glycols ,Transcriptome ,Sequencing techniques ,Cell Signaling ,Plant Resistance to Abiotic Stress ,Gene expression ,Ipomoea batatas ,lcsh:Science ,Disease Resistance ,Plant Proteins ,Genetics ,Multidisciplinary ,Dehydration ,Ecology ,food and beverages ,RNA sequencing ,Genomics ,Somatic fusion ,Plant Physiology ,Cellular Structures and Organelles ,Transcriptome Analysis ,Research Article ,Signal Transduction ,Drought Adaptation ,Drought tolerance ,Calcium-Transporting ATPases ,Plant disease resistance ,Biology ,Ipomoea ,03 medical and health sciences ,Osmotic Pressure ,Plant-Environment Interactions ,DNA-binding proteins ,Plant Defenses ,Calcium Signaling ,Gene ,Chimera ,Gene Expression Profiling ,Plant Ecology ,lcsh:R ,Ecology and Environmental Sciences ,fungi ,Biology and Life Sciences ,Proteins ,Membrane Proteins ,Computational Biology ,Cell Biology ,Plant Pathology ,Genome Analysis ,biology.organism_classification ,Research and analysis methods ,Gene expression profiling ,Molecular biology techniques ,030104 developmental biology ,lcsh:Q ,010606 plant biology & botany - Abstract
Previously, we obtained the sweetpotato somatic hybrid KT1 from a cross between sweetpotato (Ipomoea batatas (L.) Lam.) cv. Kokei No. 14 and its drought-tolerant wild relative I. triloba L. KT1 not only inherited the thick storage root characteristic of Kokei No. 14 but also the drought-tolerance trait of I. triloba L. The aim of this study was to explore the molecular mechanism of the drought tolerance of KT1. Four-week-old in vitro-grown plants of KT1, Kokei No. 14, and I. triloba L. were subjected to a simulated drought stress treatment (30% PEG6000) for 0, 6, 12 and 24 h. Total RNA was extracted from samples at each time point, and then used for transcriptome sequencing. The gene transcript profiles of KT1 and its parents were compared to identify differentially expressed genes, and drought-related modules were screened by a weighted gene co-expression network analysis. The functions of ABI-like protein and Ca2+-ATPase, two proteins screened from the cyan and light yellow modules, were analyzed in terms of their potential roles in drought tolerance in KT1 and its parents. These analyses of the drought responses of KT1 and its somatic donors at the transcriptional level provide new annotations for the molecular mechanism of drought tolerance in the somatic hybrid KT1 and its parents.
- Published
- 2018
6. HBV-Associated Postinfectious Acute Glomerulonephritis: A Report of 10 Cases
- Author
-
Yong Zhang, Feng Zheng, Guoqing Yu, Li-ping Wang, Weihua Peng, Jian Chen, and Junxia Li
- Subjects
Male ,Pulmonology ,Physiology ,Kidney Glomerulus ,030232 urology & nephrology ,Complement System ,lcsh:Medicine ,Artificial Gene Amplification and Extension ,Disease ,Immune Complex ,medicine.disease_cause ,Biochemistry ,Polymerase Chain Reaction ,0302 clinical medicine ,Glomerulonephritis ,Immune Physiology ,Medicine and Health Sciences ,lcsh:Science ,Child ,Pathology and laboratory medicine ,Multidisciplinary ,Proteinuria ,Immune System Proteins ,Acute kidney injury ,virus diseases ,Medical microbiology ,Hepatitis B ,Immune complex ,Nephrology ,030220 oncology & carcinogenesis ,Acute glomerulonephritis ,Acute Disease ,Viruses ,Female ,medicine.symptom ,Anatomy ,Pathogens ,Glomeruli ,Research Article ,Adult ,Hepatitis B virus ,Adolescent ,Immunology ,Research and Analysis Methods ,Microbiology ,03 medical and health sciences ,medicine ,Humans ,Molecular Biology Techniques ,Pathological ,Molecular Biology ,business.industry ,lcsh:R ,Viral pathogens ,Organisms ,Biology and Life Sciences ,Proteins ,Kidneys ,Renal System ,medicine.disease ,digestive system diseases ,Hepatitis viruses ,Microbial pathogens ,Immune System ,Respiratory Infections ,lcsh:Q ,business - Abstract
Postinfectious acute glomerulonephritis (PIGN) may occur after various bacterial and viral infections. Hepatitis B virus (HBV) infection is a cause of chronic glomerulonephritis. We report here 10 cases (ages 7–20 years-old) of chronic HBV carriers with acute glomerulonephritis, with positive glomerular staining of hepatitis B surface antigen, and detectable presence of HBV DNA in the glomeruli. This form of PIGN, HBV-PIGN, has not been previously identified. To further characterize clinical and pathological features of HBV- PIGN, we selected 10 cases of age-matched non-HBV PIGN for comparison. While both HBV associated PIGN and non-HBV PIGN similarly presented as proteinuria, hematuria, and hypertension, there was a trend of higher acute kidney injury and worsened prognosis in HBV-PIGN. 6 months after the onset, 4 patients with HBV associated PIGN did not show improvement from the disease, whereas all patients with non-HBV PIGN had complete or partial recovery. Pathologically, both HBV associated PIGN and non-HBV PIGN showed typical diffuse glomerular endocapillary proliferation, but HBV associated PIGN differed from classical PIGN with much fewer sub-epithelial glomerular “hump-shape” immune complex depositions. In conclusion, we have identified a novel association of HBV infection with acute glomerulonephritis.
- Published
- 2015
7. Intravascular ultrasound observation of the mechanism of no-reflow phenomenon in acute myocardial infarction
- Author
-
Longmei Wu, Xinli Tian, Jian Zhang, Yujie Shi, and Junxia Li
- Subjects
Male ,congenital, hereditary, and neonatal diseases and abnormalities ,medicine.medical_specialty ,Mechanical Thrombolysis ,medicine.medical_treatment ,Myocardial Infarction ,lcsh:Medicine ,Coronary Angiography ,Coronary circulation ,Percutaneous Coronary Intervention ,Risk Factors ,Coronary Circulation ,Internal medicine ,Intravascular ultrasound ,medicine ,Humans ,Myocardial infarction ,cardiovascular diseases ,lcsh:Science ,Ultrasonography, Interventional ,Aged ,Multidisciplinary ,medicine.diagnostic_test ,business.industry ,lcsh:R ,Percutaneous coronary intervention ,Middle Aged ,equipment and supplies ,medicine.disease ,Thrombosis ,Plaque, Atherosclerotic ,surgical procedures, operative ,medicine.anatomical_structure ,Angiography ,No reflow phenomenon ,Cardiology ,cardiovascular system ,No-Reflow Phenomenon ,Myocardial infarction complications ,Female ,lcsh:Q ,Radiology ,business ,Research Article - Abstract
Objective To study the mechanism of the no-reflow phenomenon using coronary angiography (CAG) and intravascular ultrasound (IVUS). Methods A total of 120 patients with acute myocardial infarction (AMI) who successfully underwent indwelling intracoronary stent placement by percutaneous coronary intervention (PCI). All patients underwent pre- and post-PCI CAG and pre-IVUS. No-reflow was defined as post-PCI thrombolysis in myocardial infarction (TIMI) grade 0, 1, or 2 flow in the absence of mechanical obstruction. Normal reflow was defined as TIMI grade 3 flow. The pre-operation reference vascular area, minimal luminal cross-sectional area, plaque cross-sectional area, lesion length, plaque volume and plaque traits were measured by IVUS. Results The no-reflow group was observed in 14 cases (11.6%) and normal blood-flow group in 106 cases (89.4%) based on CAG results. There was no statistically significant difference in the patients’ medical history, reference vascular area (no-flow vs. normal-flow; 15.5 ± 3.2 vs. 16.2 ± 3.3, p> 0.05) and lesion length (21.9 ± 5.1 vs. 19.5 ± 4.8, p> 0.05) between the two groups. No-reflow patients had a longer symptom onset to reperfusion time compared to normal blood-flow group [(6.6 ± 3.1) h vs (4.3 ± 2.7) h; p< 0.05] and higher incidence of TIMI flow grade< 3 (71.4% vs 49.0%, p< 0.05). By IVUS examination, the no-reflow group had a significantly increased coronary plaque area and plaque volume compared to normal blood-flow group [(13.7 ± 3.0) mm2 vs (10.2 ± 2.9) mm2; (285.4 ± 99.8) mm3 vs (189.7 ± 86.4) mm3; p< 0.01]. The presence of IVUS-detected soft plaque (57.1% vs. 24.0%, p< 0.01), eccentric plaque (64.2% vs. 33.7%, p< 0.05), plaque rupture (50.0% vs. 21.2%, p< 0.01), and thrombosis (42.8% vs. 15.3%) were significantly more common in no-reflow group. Conclusion There was no obvious relationship between the coronary risk factors and no-reflow phenomenon. The symptom onset to reperfusion time, TIMI flow grade before stent deployment, plaque area, soft plaques, eccentric plaques, plaque rupture and thrombosis may be risk factors for the no-reflow phenomenon after PCI.
- Published
- 2015
8. FSH Modulates PKAI and GPR3 Activities in Mouse Oocyte of COC in a Gap Junctional Communication (GJC)-Dependent Manner to Initiate Meiotic Resumption
- Author
-
Guankun Mao, Junxia Li, and Guoliang Xia
- Subjects
Sexual Reproduction ,MAPK/ERK pathway ,Anatomy and Physiology ,Time Factors ,lcsh:Medicine ,Stimulation ,Cell Communication ,Receptors, G-Protein-Coupled ,Mice ,Follicle-stimulating hormone ,Molecular Cell Biology ,Cyclic AMP ,Phosphorylation ,lcsh:Science ,Cumulus Cells ,Multidisciplinary ,Gap Junctions ,Phosphodiesterase ,Signaling in Selected Disciplines ,Cell biology ,Meiosis ,medicine.anatomical_structure ,Female ,Mitogen-Activated Protein Kinases ,Cell Division ,hormones, hormone substitutes, and hormone antagonists ,Research Article ,Signal Transduction ,endocrine system ,medicine.medical_specialty ,Cell signaling ,Endocrine System ,GPR3 ,Biology ,Internal medicine ,medicine ,Reproductive Endocrinology ,Animals ,Protein kinase A ,Endocrine Physiology ,lcsh:R ,Reproductive System ,Oocyte ,Cyclic Nucleotide Phosphodiesterases, Type 3 ,Enzyme Activation ,Cyclic AMP-Dependent Protein Kinase Type I ,Endocrinology ,Oocytes ,lcsh:Q ,Follicle Stimulating Hormone ,Endocrinological Signaling - Abstract
Many studies have shown that cyclic adenosine-5'-monophosphate (cAMP)-dependent protein kinase A (PKA) and G-protein-coupled receptor 3 (GPR3) are crucial for controlling meiotic arrest in oocytes. However, it is unclear how gonadotropins modulate these factors to regulate oocyte maturation, especially by gap junctional communication (GJC). Using an in vitro meiosis-arrested mouse cumulus-oocyte complex (COC) culture model, we showed that there is a close relationship between follicle-stimulating hormone (FSH) and the PKA type I (PKAI) and GPR3. The effect of FSH on oocyte maturation was biphasic, initially inhibitory and then stimulatory. During FSH-induced maturation, rapid cAMP surges were observed in both cumulus cells and oocyte. Most GJC between cumulus cells and oocyte ceased immediately after FSH stimulation and recommenced after the cAMP surge. FSH-induced maturation was blocked by PKAI activator 8-AHA-cAMP. Levels of PKAI regulatory subunits and GPR3 decreased and increased, respectively, after FSH stimulation. In the presence of the GJC inhibitor carbenoxolone (CBX), FSH failed to induce the meiotic resumption and the changes in PKAI, GPR3 and cAMP surge in oocyte were no longer detected. Furthermore, GPR3 was upregulated by high cAMP levels, but not by PKAI activation. When applied after FSH stimulation, the specific phosphodiesterase 3A (PDE3A) inhibitor cilostamide immediately blocked meiotic induction, regardless of when it was administered. PKAI activation inhibited mitogen-activated protein kinase (MAPK) phosphorylation in the oocytes of COCs, which participated in the initiation of FSH-induced meiotic maturation in vitro. Just before FSH-induced meiotic maturation, cAMP, PKAI, and GPR3 returned to basal levels, and PDE3A activity and MAPK phosphorylation increased markedly. These experiments show that FSH induces a transient increase in cAMP levels and regulates GJC to control PKAI and GPR3 activities, thereby creating an inhibitory phase. After PDE3A and MAPK activities increase, meiosis resumes.
- Published
- 2012
9. Aminoglycoside stress together with the 12S rRNA 1494C>T mutation leads to mitophagy.
- Author
-
Jialing Yu, Jing Zheng, Xiaoxu Zhao, Junxia Liu, Zhuochao Mao, Yining Ling, Danni Chen, Chao Chen, Lanlan Hui, Limei Cui, Ye Chen, Pingping Jiang, and Min-Xin Guan
- Subjects
Medicine ,Science - Abstract
Aminoglycosides as modifying factors modulated the phenotypic manifestation of mitochondrial rRNA mutations and the incomplete penetrance of hearing loss. In this report, using cybrids harboring the m.1494C>T mutation, we showed that gentamycin aggravated mitochondrial dysfunction in a combination of the m.1494C>T mutation. The m.1494C>T mutation was responsible for the dramatic reduction in three mtDNA-encoded proteins of H-strand, with the average of 39% reduction, except of the MT-ND6 protein, accompanied with 21% reduction of ATP production and increase in mitochondrial reactive oxygen species, compared with those of control cybrids. After exposure to gentamycin, 35% reduction of mitochondrial ATP production was observed in mutant cybrids with a marked decrease of the mitochondrial membrane potential. More excessive cellular reactive oxygen species was detected with stimulus of gentamycin than those in mutant cells. Under gentamycin and m.1494C>T stress together, more dysfunctional mitochondria were forced to fuse and exhibited mitophagy via up-regulated LC3-B, as a compensatory protective response to try to optimize mitochondrial function, rather than undergo apoptosis. These findings may provide valuable information to further understand of mechanistic link between mitochondrial rRNA mutation, toxicity of AGs and hearing loss.
- Published
- 2014
- Full Text
- View/download PDF
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